Venous insufficiency includes a range of conditions. As background, veins function to return blood to the central circulation and to the heart, and therefore, veins carry the blood from the farthest extremities of the body. In most cases, because veins are post-capillary, meaning the veins follow the capillaries and the antegrade circulation of the blood, the veins are at a very low pressure relative to the arterial pressure. Accordingly, the hydrodynamic forces available to return the blood to the central circulation and to the heart are low. In human physiology there are mechanisms in the circulation of the extremities to promote the return flow of venous blood to the central circulation.
Among these naturally occurring anatomical mechanisms notably in the extremities are valves distributed along the veins that act to prevent regurgitation of blood flow progressing toward the central veins. This is especially important in the lower extremities where most clinical problems are manifest because the lower extremities are hydrostatically substantially lower than the heart. The circulatory system in the lower extremities when in a dependent position must, nonetheless, convey blood back up to the central circulation against the hydrostatic pressure. Also essential, the leg muscle action of upright posture and ambulation acts to compress the veins of the deep vein system of the lower extremities and propel venous blood centrally. Further, communicating veins, also valved, conduct blood from the superficial veins into the deep veins so that muscle action serves to promote lower extremity vein blood flow generally.
In certain disease states chronic conditions can lead to compression of proximal veins and retarded return blood flow in the lower extremities, resulting in congestion of their venous systems and chronically elevated pressures for which they are not adapted. Over time, this leads to dilation of the veins that in turn causes failure of coaptation of the venous valves resulting in more congestion and swelling. This vicious cycle can progress to failure of a multiplicity of vein valves including those of the communicating veins and marked symptomatic dilation of the superficial veins. When the veins become dilated enough, all of the valves can become incompetent and in severe cases the entire function of moving blood back against the hydrostatic force can fail.
Veins are prone to this because they are thin-walled, being a low pressure vessel adapted to function at the often superficial level of a viscus or body part. This vulnerability increases with age and adverse loading conditions associated with certain functional and disease conditions. Among these are the effects of obesity and sedentary behavior that result in compression of the central veins along the posterior aspect of the pelvic bowl. That course joins the principal veins of the thorax and inferior vena cava to return blood to the heart. The weight of the abdominal contents, especially in sitting posture, can compress the veins of the pelvis, and aggravated by obesity and sedentary behavior, result in increased vein pressures in the lower extremities. As the vein pressures rise, the increase in pressure causes dilation of the veins and incompetence of their valves. In sum, as the veins dilate and the valves become incompetent, there is no way of restoring the normal caliber and architecture of the veins. As a result, the manifestations of the diseases that proceed from venous insufficiency become progressive and severe.
By way of example, complications thereafter can include lymphedema, which is partly related to the destruction of the lymphatic system that can cause the patient to become prone to infection with accompanying discomfort, and even destruction of the tissue may ensue.
Function of the lymphatic vessel system is also essential to the maintenance of fluid homeostasis in the soft tissues, including those of the lower extremities, and this function is directly influenced by the state of venous blood flow and pressure. In normal circulatory processes there is some movement of fluid from the post-capillary veins and collecting veins into the soft tissues. The contents of that fluid contains some degree of protein and formed elements of the blood (including cells). Such compositions in small quantities and in small flow can be absorbed by the lymphatics, which carry the fluid out of the tissue back into the central circulation through the lymph system. However, with chronic and excessive elevation of the vein pressure the high material content of the transudated fluid can overload the capacity of the lymphatic vessels causing them to become clogged and degraded. Destruction of portions of the lymphatic system increases the burden of what the remainder of the lymphatics have to carry, which is a degenerative cycle for the lymphatic system alone. Indeed, if the collective regional function of the lymphatics is sufficiently compromised, the patient can develop permanent retention of fluid in the tissue. Moreover, since the lymph system is also part of the means by which the immune system acts in the soft tissues, then a patient can develop a tendency to infection and damage to the tissue by virtue of congestion. Therefore, the impacts of venous insufficiency are not simply a matter of cosmetic appearance and/or discomfort, but the function of the venous system in the lower extremities is an important part of the patient's health and well-being.
Therapies to address venous insufficiency have been limited due, at least in part, to the structure of the venous system in the lower extremities. More particularly, in the lower extremities the human anatomy includes a superficial vein system and deep vein system. The deep vein system runs in the central muscle compartments of the lower extremity including the calf and thigh, such that muscle action squeezes the vein and propels the blood upward against hydrostatic pressure. Even so, if the deep veins lose their valves, for example, as can happen in the case of vein thrombosis, the patient can develop severe fluid congestion of the lower extremity. Apart from the more commonly understood superficial venous disease conditions, when the deep veins fail, there are serious consequences.
For all of the conditions that cause failure of the valves and dilatation of the superficial veins that can produce both pain and cosmetic problems by causing congestion and deformation of the skin, it has become popular to attempt to treat venous insufficiency, at least in the superficial veins.
In general, currently available forms of therapy for venous insufficiency are essentially destructive. By way of example, existing therapies exert tissue lysis effects on the vein with lasers or heat probes. Alternatively, the superficial veins are surgically removed, otherwise known as “vein stripping.”
Accordingly, current therapies to address venous insufficiency are limited, and therefore, there is a need for additional therapies to address venous insufficiency. In particular, means are needed to treat venous insufficiency by restoring venous flow and valvular competence rather than by destroying the available superficial veins. Previous designs have suffered from limitations in positional stability causing the implanted valves to lose their position and axial orientation in the vessel and, therefore, all effectiveness in valvular function. This failing is caused by anatomic factors. First, the vein walls can be compliant to the point of laxity, and second, this compliance under hydrostatic cyclic pressure loading then causes the diameter of the vessel to change dramatically with subject posture and activity. Thus, a design is needed that can maintain contact with the inner surface of the vessel and retain its axial orientation under variable hydrostatic loads.
In other disease conditions the veins of an organ or body region may themselves be of normal configuration and native function, but the circulatory pressure loads exerted upon them may be markedly elevated due to congestive conditions in the heart or obstruction of the central veins. In such conditions, such as superior vena cava syndrome or severe tricuspid valve regurgitation, a device to treat the condition would be desirable.